The future treatment of portal hypertension

Reichen, Jürg; Lebrec, Didier

doi:10.1016/j.bpg.2006.07.006

Cited by 12 publications

(11 citation statements)

References 118 publications

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“…Our next objective was to analyse whether the decreased adrenergic participation in STPH was associated with a decrease in NA release and/or vasoconstrictor response to NA. In our experimental conditions, concentration-response curves to exogenous NA were similar in segments from both groups of rats, contrasting with previous studies reporting both an increase and a decrease of vasoconstrictor response to NA [4,[18][19][20][21]; meanwhile, both basal and EFS-induced NA releases were diminished in mesenteric segments from PH rats, as also reported with reference to circulating NA [18,19]. Therefore these results explain the decrease of adrenergic function that results in the diminished vasoconstrictor response to EFS observed in STPH.…”

Section: Short-term Phcontrasting

confidence: 84%

“…In PH, and with regard to adrenergic innervation, both an increase and a decrease in vasoconstrictor response to NA have been reported [4,[18][19][20][21], as well as a downregulation of genes related to the adrenergic system and atrophy of mesenteric sympathetic innervation [22,23]. In reference to nitrergic innervation, increased involvement of neuronal NO in EFS-induced vasodilation [24] and in nNOS [neuronal NOS (nitric oxide synthase)] expression [25] has been described.…”

Section: Introductionmentioning

confidence: 92%

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Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

et al. 2011

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In the present study, we analysed possible alterations in adrenergic, nitrergic and sensory functioning in mesenteric arteries from rats at 1 and 21 months after partial portal vein ligation, and the mechanisms involved in these alterations, if any. For this purpose, we analysed the vasoconstrictor response to EFS (electrical field stimulation) and the effect of the α-antagonist phentolamine, the NOS (nitric oxide synthase) inhibitor L-NAME (N(G)-nitro-L-arginine methyl ester) and the CGRP (calcitonin gene-related peptide) receptor antagonist CGRP-(8-37) in mesenteric segments from ST (short-term; 1 month) and LT (long-term; 21 months) SO (sham-operated) and pre-hepatic PH (portal hypertensive) rats. The vasomotor responses to NA (noradrenaline), the NO donor DEA-NO (diethylamine NONOate) and CGRP were analysed. NA, NO and CGRP releases were measured. Phospho-nNOS (neuronal NOS) expression was studied. The vasoconstrictor response to EFS was decreased in STPH animals. Phentolamine decreased this vasoconstrictor response more strongly in SO animals. Both L-NAME and CGRP-(8-37) increased vasoconstrictor response to EFS more strongly in PH than SO segments. PH did not modify vasomotor responses to NA, DEA-NO or CGRP, but it decreased NA release while increasing those of NO and CGRP. Phospho-nNOS expression was increased by PH. In LTPH, no differences were observed in vasoconstrictor response to EFS, vasomotor responses or neurotransmitter release when compared with age-matched SO animals. In conclusion, the mesenteric innervation may participate in the development of the characteristic hyperdynamic circulation observed in STPH through the joint action of decreased adrenergic influence, and increased nitrergic and sensory innervations influences. The participation of each innervation normalizes under conditions of LTPH.

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Section: Short-term Phcontrasting

confidence: 84%

Section: Introductionmentioning

confidence: 92%

Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

et al. 2011

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“…These neurotoxic substances may then contribute to morphologic changes in astrocytes. This may lead to increased intracranial pressure and, potentially, brain herniation [37, 38]. Therapy of HE is directed primarily at reducing ammonia generation and increasing its detoxification.…”

Section: Role Of Cytokines In Liver Complicationsmentioning

confidence: 99%

“…In the future, as new hypotheses are generated, tested, and when found to be lacking, either modified or rejected, further progress must be made. Because effective therapy is based on sound biology, as we continue to gain a better understanding of the basic mechanisms involved in this syndrome, we undoubtedly will develop new and effective therapeutic strategies for the benefit of our patients [37]. …”

Section: Cytokines In Regeneration and Repair Of Aclfmentioning

confidence: 99%

Role of Cytokines in the Pathophysiology of Acute-on-Chronic Liver Failure

Liu¹

2009

Blood Purif

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Background: This is the first ever decade which has witnessed the emergence of a highly lethal condition termed acute-on-chronic liver failure (ACLF), which today is the leading cause of death compared to acute and chronic liver failure. However, the complex pathophysiology of ACLF remains poorly understood. This article will attempt to summarize recent progress in the understanding of the mechanisms of cytokines in ACLF. Methods: The search terms used on PubMed were cytokines, liver injury, complications of liver disease, and hepatic progenitor cell. Results: Cytokines play a significant role in the pathophysiology of ACLF including hepatocellular death, extrahepatic complications and hepatocyte regeneration. The tissue-damaging mechanisms of cytokines are closely related to their hepatocyte proliferation and regeneration function. Conclusions: It remains a challenge to selectively prevent the detrimental effects of cytokines. To design interventions which selectively target the detrimental effects of cytokines, a detailed understanding of cytokines in the pathophysiology ACLF is critical.

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“…By combining the "backward flow" and the "forward flow" theory together, this would furnish a better understanding of the pathogenesis of PHT [24,25] . In the "forward flow" theory, the pathogenesis of PHT may be primarily attributed to initiation factors, including dilation of peripheral vessels, decrease in peripheral vascular resistance and mean arterial pressure, increase in blood volume, splanchnic blood flow and cardiac output, and development of systemic hyperdynamic circulatory syndrome (HCS) [23,26] . HCS plays an important role in the maintenance of PHT and is also a primary cause for the development of sodium-water retention, ascites, hepato-renal and hepato-pulmonary syndromes.…”

Section: A B Cmentioning

confidence: 99%

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

Liang¹,

Deng²,

Lin³

et al. 2009

WJG

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AIM:To investigate the inhibitory effect of natural taurine (NTau) on portal hypertension (PHT) in rats with experimentally-induced liver cirrhosis (LC). METHODS:Experimentally-induced LC Wistar rats (20 rats/group) were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure (PVP), portal venous resistance (PVR), portal venous flow (PVF), splanchnic vascular resistance (SVR) and mean arterial pressure (MAP). Vasoactive substance levels including nitric oxide (NO), nitric oxide synthase (NOS) and cyclic guanosine monophosphate (cGMP) were also measured. Histological investigation of type Ⅰ and Ⅲ collagen (COL Ⅰ and Ⅲ) and transforming growth factor-β1 (TGF-β1) was also performed. RESULTS:

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The future treatment of portal hypertension

Cited by 12 publications

References 118 publications

Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

Effect of short- and long-term portal hypertension on adrenergic, nitrergic and sensory functioning in rat mesenteric artery

Role of Cytokines in the Pathophysiology of Acute-on-Chronic Liver Failure

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

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